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What Causes Kussmaul Respirations In Dka?

Abnormal Breathing Patterns

Abnormal Breathing Patterns

Apnea Absence of breathing. (Ap-knee-a) Eupnea Normal breathing (Eup-knee-a) Orthopnea Only able to breathe comfortable in upright position (such as sitting in chair), unable to breath laying down, (Or-thop-knee-a) Dyspnea Subjective sensation related by patient as to breathing difficulty Paroxysmal nocturnal dyspnea - attacks of severe shortness of breath that wakes a person from sleep, such that they have to sit up to catch their breath - common in patient's with congestive heart failure. Hyperpnea Increased volume with or without and increased frequency (RR), normal blood gases present. Hyperventilation "Over" ventilation - ventilation in excess of the body's need for CO2 elimination. Results in a decreased PaCO2, and a respiratory alkalosis. Hypoventilation "Under" ventilation - ventilation that is less than needed for CO2 elimination, and inadequate to maintain normal PaCO2. Results in respiratory acidosis. Can be a slow rate with normal tidal volumes such that the total minute ventilation is inadequate. Can be a normal rate but with such low tidal volumes that air exchange is only in the dead space and not effective. Tachypnea Increased frequency without blood gas abnormality Kussmaul's Respiration Kussmaul's respiration. Increased rate and depth of breathing over a prolonged period of time. In response to metabolic acidosis, the body's attempt to blow off CO2 to buffer a fixed acid such as ketones. Ketoacidosis is seen in diabetics. Cheyne-Stokes respirations (CSR) Gradual increase in volume and frequency, followed by a gradual decrease in volume and frequency, with apnea periods of 10 - 30 seconds between cycle. Described as a crescendo - decrescendo pattern. Characterized by cyclic waxing and waning ventilation with apnea gradually giving way to hyperpneic brea Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

Dka Vs Hhs (hhns) Nclex Review

Dka Vs Hhs (hhns) Nclex Review

Diabetic ketoacidosis vs hyperglycemic hyperosmolar nonketotic syndrome (HHNS or HHS): What are the differences between these two complications of diabetes mellitus? This NCLEX review will simplify the differences between DKA and HHNS and give you a video lecture that easily explains their differences. Many students get these two complications confused due to their similarities, but there are major differences between these two complications. After reviewing this NCLEX review, don’t forget to take the quiz on DKA vs HHNS. Lecture on DKA and HHS DKA vs HHNS Diabetic Ketoacidosis Affects mainly Type 1 diabetics Ketones and Acidosis present Hyperglycemia presents >300 mg/dL Variable osmolality Happens Suddenly Causes: no insulin present in the body or illness/infection Seen in young or undiagnosed diabetics Main problems are hyperglycemia, ketones, and acidosis (blood pH <7.35) Clinical signs/symptoms: Kussmaul breathing, fruity breath, abdominal pain Treatment is the same as in HHNS (fluids, electrolyte replacement, and insulin) Watch potassium levels closely when giving insulin and make sure the level is at least 3.3 before administrating. Hyperglycemic Hyperosmolar Nonketotic Syndrome Affects mainly Type 2 diabetics No ketones or acidosis present EXTREME Hyperglycemia (remember heavy-duty hyperglycemia) >600 mg/dL sometimes four digits High Osmolality (more of an issue in HHNS than DKA) Happens Gradually Causes: mainly illness or infection and there is some insulin present which prevents the breakdown of ketones Seen in older adults due to illness or infection Main problems are dehydration & heavy-duty hyperglycemia and hyperosmolarity (because the glucose is so high it makes the blood very concentrated) More likely to have mental status changes due to severe dehydrat Continue reading >>

Cheyne Stokes Breathing And Other Abnormal Respiration

Cheyne Stokes Breathing And Other Abnormal Respiration

Cheyne Stokes breathing is a type of abnormal breathing. It’s characterized by a gradual increase in breathing, and then a decrease. This pattern is followed by a period of apnea where breathing temporarily stops. The cycle then repeats itself. Normal breathing, the process of moving air in and out of the lungs 12 to 20 times per minute, is something most people seldom think about. However, abnormal breathing like Cheyne Stokes is serious and may be frightening. When does it most likely occur? According to research, Cheyne Strokes breathing can happen while you’re awake, but is more common during sleep. It may happen more during non-rapid eye movement (NREM) sleep than rapid eye movement (REM) sleep. When Cheyne Stokes occurs during sleep, it’s considered a form of central sleep apnea with an extended period of fast breathing (hyperventilation). Central sleep apnea causes you to stop breathing briefly and increases the levels of carbon dioxide in your body. Cheyne Stokes is usually related to heart failure or stroke. It may also be caused by: brain tumors traumatic brain injuries high altitude sickness encephalitis increased intercranial pressure chronic pulmonary edema People who are dying often experience Cheyne Stokes breathing. This is a natural effect of the body’s attempt to compensate for changing carbon dioxide levels. While it may be distressing to those who witness it, there’s no evidence Cheyne Stokes is stressful for the person experiencing it. Both Kussmaul breathing and Cheyne Stokes breathing are characterized by fast breathing and too much carbon dioxide in the body, but that’s where their similarities end. Kussmaul breathing doesn’t alternate between fast and slow breathing or cause breathing to stop like Cheyne Stokes does. Instead, it’ Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

DKA is an acute complication of diabetes mellitus (usually type 1 diabetes) characterized by hyperglycemia, ketonuria, acidosis, and dehydration. Insulin deficiency prevents glucose from being used for energy, forcing the body to metabolize fat for fuel. Free fatty acids, released from the metabolism of fat, are converted to ketone bodies in the liver. Increase in the secretion of glucagon, catecholamines, growth hormone, and cortisol, in response to the hyperglycemia caused by insulin deficiency, accelerates the development of DKA. Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes, with losses in potassium, sodium, phosphate, and water. Serum glucose level is usually elevated over 300 mg/dL; may be as high as 1,000 mg/dL. Serum bicarbonate and pH are decreased due to metabolic acidosis, and partial pressure of carbon dioxide is decreased as a respiratory compensation mechanism. Serum sodium and potassium levels may be low, normal, or high due to fluid shifts and dehydration, despite total body depletion. Urine glucose is present in high concentration and specific gravity is increased, reflecting osmotic diuresis and dehydration. Observe for cardiac changes reflecting dehydration, metabolic acidosis, and electrolyte imbalance- hypotension; tachycardia; weak pulse; electrocardiographic changes, including elevated P wave, flattened T wave or inverted, prolonged QT interval. Administer replacement electrolytes and insulin as ordered. Flush the entire I.V. infusion set with solution containing insulin and discard the first 50 mL because plastic bags and tubing may absorb some insulin and the initial solution may contain decreased concentration of insulin. Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

Acid-base Physiology

Acid-base Physiology

An outline of management is presented: this should be tailored to individual circumstances. Management of DKA has passed through 3 stages in the last 100 years: Stage 1: Preinsulin era (Feature: mortality of 100%) Stage 2: High dose insulin regime (Feature: mortality down to 10% but metabolic complications due to the treatment) Stage 3 (the present): Low dose insulin regime (Feature: low mortality) Mortality with the low dose insulin regime is down to about 2 to 5% overall. In older patients with DKA precipitated by a major medical illness (eg acute pancreatitis, myocardial infarction, septicaemia), the mortality rate is still high due to the severity of the precipitating problem. Restore normal carbohydrate and lipid metabolism Management can be considered in terms of emergency and routine components. Protect by intubation with a cuffed tube if patient is significantly obtunded. Consider placing a nasogastric tube in all patients. Intubation may be necessary for airway protection or ventilation (eg if aspiration, coma, pneumonia, pulmonary oedema, acute pancreatitis and ARDS) but this is not common. Maintain compensatory hyperventilation in intubated patients Patients with metabolic acidosis (eg severe DKA) have marked hyperventilation (ie respiratory compensation, Kussmaul respirations) and typically low arterial pCO2 levels. If intubated and ventilated, ventilatory parameters (tidal volume and rate) need to be set to continue a high minute ventilation. If this is not done and pCO2 is inappropriately high, a severe acidaemia and consequent severe cardiovascular collapse may occur This is a particular problem in all situations where a patient with a compensated metabolic acidosis is intubated and ventilated. The rule of thumb is to aim for a pCO2 level of 1.5 times th Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>

Kussmaul Respirations Dka Causes Metabolic Acidosis

Kussmaul Respirations Dka Causes Metabolic Acidosis

Kussmaul respirations DKA causes metabolic acidosis The kidneys hold on to Kussmaul respirations dka causes metabolic acidosis 100% (1) 1 out of 1 people found this document helpful This preview shows page 8 - 10 out of 10 pages. Kussmaul respirations. DKA causes metabolic acidosis. The kidneys hold on to hydrogen ions and thus are in excess in the blood. The body compensates by attempting to blow off extra acid in the form of carbon dioxide. Kussmaul respirations are deep and labored and at a fast rate to ensure the body is rid of carbon dioxide (McCance & Huether, 2014).Fruity breath. When the body cannot burn glucose for fuel, because glucose is in the blood and not the cells, it resorts to burning fats instead. Lipolysis produces ketones. The 8 TYPE 1 DIABETES MELLITUS DIABETIC KETOACIDOSISbuild up of ketones in the blood causes breath to smell a bit sweet or like acetone, a type of ketone. (what does bad breath have to do with diabetes? Peggy pletcher)Weight loss. Type 1 Diabetes requires the body to gain energy from fats and proteins rather than glucose in the presence of insulin deficiency. When fats and proteins are broken down, the body loses mass (McCance & Huether, 2014). Weight loss also occurs due to fluid and water loss during diuresis (McCance & Huether, 2014).Hyperglycemia. Pancreatic beta cells produce insulin and alpha cells produce glucagon. Insulin normally suppresses glucagon secretion. However, type 1 Diabetes causes destruction of both pancreatic alpha and beta cells. The lack of insulin and excess of glucagon contribute to excess glucose in the blood (McCance & Huether, 2014).Increased BUN. Increased Creatinine.Hypotension. Dehydration causes low volume to the blood. Less volume equals less pressure needed to pump blood throughout the body (McCa Continue reading >>

Diabetic Emergencies: Ketoacidosis

Diabetic Emergencies: Ketoacidosis

Our flight crew was dispatched to a small local hospital for a 58 year old male with an altered level of consciousness and elevated blood sugar. His son had found him unresponsive on the couch and called EMS for help. While en route to the local hospital a bedside glucose was checked reporting "high." His respiratory rate was 36 and his heart rate was in the 150s. He was slow to respond, but woke to verbal commands and was orientated to person only. At the hospital, another bedside glucose returned "high" and he received 10 units of insulin IV. A foley catheter was inserted draining 1400 ml of urine immediately. The flight crew arrived to find our patient’s LOC without change. Pupils were equal at 3 mm, and sluggish in response to light. Mucous membranes were dry. He had a respiratory rate of 36 breaths per minute and shallow. His lung sounds were clear and equal bilateral. An incision at his right shoulder from a surgery one week ago appeared well healed with no redness or signs of infection. Lab results available at the time of transport were limited to: Glucose — 799 mg/dl CO2 — 3.1 mEq/L ph — 6.77 (venous) Fluid intake — 800 ml 0.9% sodium chloride Urine output — 1400 ml The only medication given so far was regular insulin 10 units IV. Definition: Diabetes mellitus is a chronic disease comprised of a group of hyperglycemic disorders, characterized by high serum glucose, and disturbances of carbohydrate and lipid metabolism. Type 1 The patient is usually less than 40 years old at the time of onset. Peak age of onset is 10 to 14 years old. They are typically lean and ketosis prone. Plasma insulin levels are low to absent. Type 2 This patient is usually 45 to 65 years old at the time of onset. These patients are typically overweight, with normal to high ins Continue reading >>

Respiratory System And Diabetes

Respiratory System And Diabetes

Tweet The respiratory system is the system of organs that allow the body to take in oxygen and expel carbon dioxide, this process is known as gaseous exchange. We generally breathe between 12 and 20 times a minute. There are a number of complications of diabetes that can negatively affect our breathing. Parts of the respiratory system The following parts of the body make up the respiratory system: Mouth and nose Trachea (windpipe) Lungs Diaphragm How the respiratory system works Breathing is usually initiated by contraction of the diaphragm, a muscle which separates the chest cavity from the abdomen. Tweet Type 2 diabetes mellitus is a metabolic disorder that results in hyperglycemia (high blood glucose levels) due to the body: Being ineffective at using the insulin it has produced; also known as insulin resistance and/or Being unable to produce enough insulin Type 2 diabetes is characterised by the body being unable to metabolise glucose (a simple sugar). This leads to high levels of blood glucose which over time may damage the organs of the body. From this, it can be understood that for someone with diabetes something that is food for ordinary people can become a sort of metabolic poison. This is why people with diabetes are advised to avoid sources of dietary sugar. The good news is for very many people with type 2 diabetes this is all they have to do to stay well. If you can keep your blood sugar lower by avoiding dietary sugar, likely you will never need long-term medication. Type 2 diabetes was formerly known as non-insulin-dependent or adult-onset diabetes due to its occurrence mainly in people over 40. However, type 2 diabetes is now becoming more common in young adults, teens and children and accounts for roughly 90% of all diabetes cases worldwide. How serious Continue reading >>

Breathsounds - Because At The Head Of Every Team Is A Respiratory Therapist

Breathsounds - Because At The Head Of Every Team Is A Respiratory Therapist

Breathing isnt just a matter ofinhaling the good air and exhaling the bad used air. The entire respiratorypattern is important. Rate, depth, timing, and consistency of breaths are allimportant to the delicate balance of respiration and metabolism. Certain illnesses or injuries cancause changes in the breathing pattern. Changes other than the typical fast orslow breathing that is most common with many conditions. Below are some of theless common breathing patterns that make many healthcare professionals askthemselves Hey, what is that pattern anyway? This breathing pattern is characterized by periods of respirations during which the spontaneous tidal volume starts shallow and progressively gets deeper with each breathe, then gets progressively more shallow with each breathe. This is followed by a period of apnea that can last anywhere from 15 seconds to 120 seconds. This cycle is repeated over and over. Causes: Cheyen-Stokes breathing is often caused by strokes, traumatic brain injuries, brain tumors, carbon dioxide poisoning, and metabolic encephalopathy. This pattern can also be seen in healthy patients experiencing first-time high altitude sickness, and can also be a normal side effect of IV morphine administration. Biot's Breathing (aka "Cluster" breathing): Biot's breathing is characterized by periods, or "clusters", of fairly rapid respirations of close to equal depth followed by reular periods of apnea that can last between 15 seconds to 120 seconds. Biot's breathing is very imilar to Cheyen-Stokes except the spontaneous tidal volume is equal throughout the period of respiration. Causes: Biot's breathing is usually caused by damage to the medulla oblongata by stroke (CVA) or trauma, or pressure on the medulla due to uncal or tenorial herniation. Biot's breathing Continue reading >>

Ketoacidosis In Cats – Causes, Symptoms & Treatment

Ketoacidosis In Cats – Causes, Symptoms & Treatment

Ketoacidosis in cats at a glance Ketoacidosis is a serious complication of diabetes in which ketones and blood sugar levels build up in the body due to insufficient levels of insulin which is required to move glucose into the cells for energy. As a result, the body uses fat as an alternate energy source which produces ketones causing the blood to become too acidic. Common causes include uncontrolled diabetes, missed or insufficient insulin, surgery, infection, stress and obesity. Symptoms of ketoacidosis include increased urination and thirst, dehydration, nausea, diarrhea, confusion, rapid breathing which may later change to laboured breathing. What is diabetic ketoacidosis? Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes characterised by metabolic acidosis (increased acids in the blood), hyperglycemia (high blood glucose) and ketonuria (ketones in the urine). It is caused by a lack of or insufficient amounts of insulin which is required to move glucose from the bloodstream and into the cells to be used for energy. When this occurs, the body begins to search for alternate sources of energy and begins to break down fat. When fat is broken down (metabolised) into fatty acids, waste products known as ketones (acetoacetate, beta-hydroxybutyrate, acetone) are released from the liver and accumulate in the bloodstream (known as ketonemia). This causes the blood to become too acidic (metabolic acidosis). As well as metabolic acidosis, ketones also cause central nervous depression.The body will try to get rid of the ketones by excreting them out of the body via the urine, increased urine output leads to dehydration, making the problem worse. Meanwhile, the unused glucose remains in the bloodstream, resulting in hyperglycemia (high blood sugar).Insulin Continue reading >>

Diabetic Ketoacidosis And Patho

Diabetic Ketoacidosis And Patho

pathophysiology ketogenesis due to insulin deficiency leads to increased serum levels of ketones anad ketonuria acetoacetate, beta-hydroxybutyrate; ketone bodies produced by the liver, organic acids that cause metabolic acidosis respiration partially compensates; reduces pCO2, when pH < 7.2, deep rapid respirations (Kussmaul breathing) acetone; minor product of ketogenesis, can smell fruity on breath of ketoacidosis patients elevated anion gap Methanol intoxication Uremic acidosis Diabetic ketoacidosis Paraldehyde ingestions Intoxicants (salicyclate, ethylene glycol, nipride, epinephrine, norepinephrine) Lactic acidosis (drug induced; didanosine, iron, isoniazid, metformin, zidovudine) Ethanol ketoacidosis Severe renal failure starvation Blood glucose regulation (6) 1. When blood glucose levels rise above a set point, 2. the pancreas secretes insulin into the blood. 3. Insulin stimulates liver and muscle cells to make glycogen, dropping blood glucose levels. 4. When glucose levels drop below a set point, 5. the pancreas secretes glucagon into the blood. 6. Glucagon promotes the breakdown of glycogen and the release of glucose into the blood. (The pancreas signals distant cells to regulate levels in the blood = endocrine function.) Insulin and Glucagon (Regulation) (10) 1. High blood glucose 2. Beta cells 3. Insulin 4. Glucose enters cell 5. Blood glucose lowered 6. Low blood glucose 7. Alpha cells 8. Glucagon 9. Liver releases glucose from glycogen 10. Blood glucose raised What is the manifestations (symptoms) of Type 1? (10) 1. Extreme thirst 2. Frequent urination 3. Drowsiness, lethargy 4. Sugar in urine 5. Sudden vision change 6. Increased appetite 7. Sudden weight loss 8. Fruity, sweet, or wine like odor on breath 9. Heavy, laboured breathing 10. Stupor, unconscious Continue reading >>

Diabetic Ketoacidosis With Pneumomediastinum: A Case Report

Diabetic Ketoacidosis With Pneumomediastinum: A Case Report

Diabetic ketoacidosis with pneumomediastinum: a case report Cases Journal volume2, Articlenumber:8095 (2009) Cite this article An 18-year-old male with type 1 diabetes mellitus presented to the emergency department after one day of lethargy and vomiting. Physical examination revealed a dehydrated male with tachycardia and Kussmaul's respiration. There was subcutaneous emphysema in both supraclavicular regions. Chest auscultation revealed a positive Hamman's sign. Laboratory investigation was significant for metabolic acidosis with venous blood pH 7.08. Plasma glucose was 1438 mg/dl; ketones were present in the urine. Chest X-ray showed subcutaneous emphysema and pneumomediastinum, which resolved spontaneously within 72 hours of initiation of treatment for diabetic ketoacidosis. Pneumomediastinum is an uncommon complication of diabetic ketoacidosis. Recognizing that severe diabetic ketoacidosis may cause pneumomediastinum allows for expedient management. An 18-year-old African-American male with type 1 diabetes mellitus presented to the emergency department with a one-day history of lethargy and vomiting. Clinical examination revealed a dehydrated male with heart rate of 120 beats/min and a blood pressure of 136/66 mmHg. He was tachypneic with a respiratory rate of 35/minute; the pattern was characteristic of Kussmaul's respiration. There was subcutaneous emphysema in both supraclavicular areas. Auscultation of the chest revealed a crunching noise over the cardiac apex and the left sternal border, synchronous with each cardiac beat (Hamman's sign). Laboratory investigation revealed a metabolic acidosis with venous blood pH 7.08. Plasma glucose was 1438 mg/dl and bicarbonate < 5 mmol/l; ketones were present in the urine. Chest X-ray showed subcutaneous emphysema as well Continue reading >>

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